Some proposed mechanisms include uremic neuropathy, skin or nerve inflammation due to kidney failure-associated chronic systemic inflammation, an increase in activity of [mu]-opioid receptors due to kidney failure (Simonsen et al., 2017), or accumulation of pruritogenic
substances (Manenti, Tansinda & Vaglio, 2009).
Lam, "Activation of eosinophils interacting with dermal fibroblasts by pruritogenic
cytokine IL-31 and alarmin IL-33: implications in atopic dermatitis," PLoS One, vol.
Hara et al., "Antimicrobial peptides human [beta]-defensins and cathelicidin LL-37 induce the secretion of a pruritogenic
cytokine IL-31 by human mast cells," The Journal of Immunology, vol.
A possible explanation to this phenomenon is that the inflammatory process of active vitiligo promotes pruritogenic
cytokines and induces itch.
IL-31 has been identified as a pruritogenic
cytokine1), and reported to be involved in the generation of pruritus in atopic dermatitis and hemodialysis2,3).
"Mu receptors mediate mast cell degranulation and have direct central and peripheral pruritogenic
effects, while kappa receptors mediate opposing, antipruritic effects," she said.
The incidence of pruritus decreased significantly as the duration of dialysis increased probably due to clearance of pruritogenic
substances by haemodialysis.
(2003), pruritus occurring with atopic dermatitis is classified as neurogenic caused by pruritogenic
factors such as histamine, serotonin, trypase affecting nervous system.
Chronic pruritus, secondary to abnormal bile flow and retention of pruritogenic
chemicals, including bile acids, usually heralds decompensation of the liver disease.
This hypothesis has been demonstrated on the grounds of three fundamental reasons: 1) pruritogenic
effect secondary to increased opioid tone; 2) increased cerebral opioid agonism as a cause of pruritus in patients with liver disorders; and 3) reduced pruritus as a result of opioid antagonism (2,3).
Traditional treatment with antihistamines is only useful for the sedative effect, however recent advances in understanding the neurophysiology of itch have led to new therapies targeted at different pruritogenic
mechanisms including opioid antagonists (e.g.
To precisely measure itch in animal behavioral experiments, we should focus on itch-related behaviors that are elicited only by pruritogenic
stimuli but not by other sensory stimuli like pain.